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Varicella-zoster virus, shingles and postherpetic neuralgia

Ann Shuttleworth, BA.

Freelance Health Journalist

Shingles is an acute unilateral and segmental inflammation of the dorsal root ganglia. It is caused by a reactivation of the chickenpox virus (varicella) some time after the primary infection. Most patients recover fully, except for possible scarring. However, a few continue to suffer pain after the shingles rash has healed. This is known as postherpetic neuralgia.

Shingles is an acute unilateral and segmental inflammation of the dorsal root ganglia. It is caused by a reactivation of the chickenpox virus (varicella) some time after the primary infection. Most patients recover fully, except for possible scarring. However, a few continue to suffer pain after the shingles rash has healed. This is known as postherpetic neuralgia.

Although it is the most common condition affecting the nervous system, shingles is not a notifiable disease, so there is no accurate data on its incidence. It has been variously estimated to affect 120 000-250 000 people a year in the UK (Johnson, 1995; Medinfo, 2003). It is primarily found in adults over the age of 50, and incidence increases with age. About 20% of people who have had chickenpox develop shingles at some time (Cunningham and Dworkin, 2000), but it seldom recurs.

After primary infection resulting in chickenpox, the virus, also known as the varicella-zoster virus (VZV), migrates along the sensory axons towards the dorsal horn, where it can lie dormant in the dorsal root ganglion for decades. During this time it is asymptomatic, and the patient will be unaware it is there.

It is unclear what precipitates reactivation of the virus, but it is likely to be linked to a decrease in cell-mediated immunity - for example, with increasing age, HIV infection or illness. The reactivated virus travels via the nerve paths to the skin, resulting in localised painful vesicular lesions in the area served by the affected dermatomes. The lesions often spread unilaterally on the thorax or vertically over the arms or legs, although any part of the body or head can be affected.

Onset is characterised by a burning or tingling sensation on the nerve paths the virus is travelling along, typically accompanied by malaise and fever (Andersen, 2002). Pain, which can range from mild to severe, usually begins two to five days before the rash emerges, although it can begin up to three weeks before. The pain can be continuous or intermittent and usually lasts for one to four weeks. The combined effects of pain and general malaise can make shingles extremely debilitating.

Up to two weeks after the onset of symptoms small, red nodular skin lesions with a similar appearance to chickenpox erupt around the affected dermatome and quickly turn into blisters filled with clear liquid or pus. The blisters burst and form scabs, which fall off after two to three weeks if left undisturbed. If the lesions are ruptured they can become infected and, in severe cases, may lead to the enlargement of lymph nodes in the affected area. Scarring is also more likely if the lesion is damaged.

The fluid in the shingles blisters contains the virus, so people who have not had chickenpox should avoid people with shingles until the blisters have dried. If they come into direct contact with the infected fluid they can contract chickenpox. People with compromised immune systems are at particular risk, such as those taking systemic steroids, who have undergone chemotherapy or a transplant or have HIV infection.

Complications
While most patients make a full recovery, complications can occur. The most common is postherpetic neuralgia. Others include:

- Ophthalmic zoster - this may cause conjunctivitis, keratitis and, rarely, uveitis, acute retinal necrosis and cataract

- Motor zoster - this can include facial paralysis

- Autonomic zoster - this may progress to urinary retention

- Zoster encephalomyelitis

- Purpura fulminans - tissue loss may be extensive

- Disseminated zoster - this is more common in immunocompromised people and can be life-threatening

- Acute retinal necrosis - this can lead to retinal detachment

- Bacterial superinfection.

Most patients with shingles can be treated by the primary care team. However, hospital admission or specialist referral is recommended in a number of situations:

- Hospital admission is required if severe complications such as encephalitis or dissemination develop

- Specialist advice is required for people who are immunocompromised

- Ophthalmic referral is required for people with ophthalmic shingles if a red eye or other sign of ocular involvement occurs.

Postherpetic neuralgia
Postherpetic neuralgia (PHN) is pain that continues beyond the normal healing time of the shingles rash. It is usually self-limiting, but in some people it can be prolonged or persist indefinitely. The incidence depends on the definition used, but data suggest there are 25 000 new UK cases each year, and an annual prevalence approaching 50 000 (Bowsher et al, 1997). Around 10-25% of patients with pain one month post-shingles have pain a year later (Ragozzino et al, 1982).

While there is no way of determining which patients with shingles will develop PHN, its incidence increases dramatically with age. Other risk factors include pain preceding the rash, greater acute pain severity, greater rash severity, sensory dysfunction in the affected dermatome during shingles, an extended rash period, a rash on the face or lower back, and being female (Kanazi et al, 2000; Johnson, 2003).

The pain in PHN is severe and can have a devastating effect on patients' quality of life, often leading to sleep disturbance, anorexia and loss of libido. It has been described as a constant burning, throbbing or aching, with intermittent shooting or stabbing sensations. Itching or numbness in the scars is often present (Scott, 2000). Patients often experience hypersensitivity of the skin (allodynia), in which minor stimuli such as movement of clothes or a draught can cause pain.

People who suffer long-term pain such as PHN are four times more likely to suffer from anxiety and depressive disorders and twice as likely to have their ability to work severely compromised than those without pain (Gureje et al, 1998). Psychological services such as those based in pain clinics may help patients to develop pain-coping strategies if pain relief is ineffective.

The panel (left) discusses treatment options. Management of PHN can be difficult with traditional analgesics, as the shingles virus can severely damage the nerve before the patient seeks help. Specific analgesic regimens for treating nerve pain may be required. Treatment by the primary care team may be enough. However, referral to a specialist pain clinic should be considered if pain relief is inadequate despite treatment with amitriptyline.

SIGNS AND SYMPTOMS
Prodromal phase of shingles:

- Paraesthesia and pain over the affected dermatome (two days to three weeks before onset of rash)

- Continuous or intermittent localised pain (varies from superficial to severe)

Acute shingles:

- Erythematous, maculopapular lesions evolving into a vesicular rash

- New lesions forming for three to five days, with scabbing four to seven days

- Rash is usually confined to one or more dermatomes; usually unilateral

- Thoracic dermatomes are usually involved, particularly T5 and T6

- Pain over the affected area

- Possible mild systemic illness (low-grade pyrexia, malaise)

Postherpetic neuralgia

- Continuing pain after shingles resolves

- Typically localised to the dermatome affected by shingles

- Scarring or hypopigmentation of skin affected by shingles possible.

DIFFERENTIAL DIAGNOSIS FOR RASH
Bacterial impetigo; herpes simplex; eczema herpeticum; coxsackie virus; pemphigoid

DIFFERENTIAL DIAGNOSIS FOR PAIN
- Pathology in vertebra, underlying bone, muscle or viscera (trauma, fracture, inflammation, infection, neoplasm)

- Diabetic mononeuritis

- Cardiac ischaemia

- Pleurisy

- Tabes dorsalis (a form of neurosyphilis).

TREATMENT FOR SHINGLES
Systemic antivirals

These can be effective if begun within 72 hours of the onset of the rash (Beutner, 1995). They are recommended for (Scott, 2000):

- All patients with ophthalmic zoster

- All immunosuppressed patients

- All patients aged over 55

- All patients with disseminated zoster.

Skin care

Skin hygiene is important to prevent secondary infection. If the lesions are weeping, raw or sticking to bedding and clothing, non-adherent dressings should be used. These symptoms often indicate a secondary infection. Some patients find calamine lotion, wet dressings and ice packs provide short-term relief from burning and itching.

Analgesia

Acute shingles pain can be severely debilitating, and effective pain relief is vital. The World Health Organization three-step analgesic ladder is a useful model (WHO, 1990):

- Step 1. Non-opioid

- Step 2. Weak opioid combined with a non-opioid

- Step 3. Strong opioid with or without a non-opioid.

An adjuvant analgesic such as low-dose amitriptyline, may be required at any step. Oral non-steroidal anti-inflammatories seem to be of little benefit for acute shingles pain.

TREATMENT FOR PHN
Skin hypersensitivity

This is common in PHN and may be reduced by wearing natural fibres, while a protective layer such as clingfilm or 'plastic skin' may be helpful.

Pain

Cold packs may provide short-term relief. Paracetamol with or without codeine is usually effective for mild to moderate pain. While opioids are useful, there is concern about the use of strong opioids as chronic use is likely to be required. Tricyclic antidepressants are effective for many patients: amitriptyline is the drug of choice, with nortriptyline preferred if this is ineffective or not tolerated. Anticonvulsants have also been effective in reducing PHN pain, particularly gabapentin and carbamazepine.

Psychological distress

Long-lasting PHN can result in depression, which may require specific management.

Andersen, F. (2002)Shingles (herpes zoster). Available at: www.netdoctor.co.uk

Beutner, K.R. (1995)Valaciclovir compared with acyclovir for improved therapy for Herpes zoster in immunocompetent adults. Antimicrobial Agents and Chemotherapy 39: 7, 1546-1553.

Bowsher, D., Friedman, D.J., Forszpaniak, C. et al. (1997)The management of postherpetic neuralgia. Postgraduate Medical Journal 73: 623-629.

Cunningham, A.L., Dworkin, R.H. (2000)The management of postherpetic neuralgia. British Medical Journal 321: 7264, 778-779.

Gureje, O., Von Korff, M., Simon, G., Gater, R. (1998)Persistent pain and well-being: a World Health Organization study on primary care. Journal of the American Medical Association 280: 2, 147-151.

Johnson, R.W. (1995)The future of predictors, prevention and therapy in postherpetic neuralgia. Neurology 45: 12, S8, 70-71.

Johnson, L. (2003)Effective pain management of postherpetic neuralgia. Nursing Times 99: 10, 32-34.

Kanazi, G.E., Johnson, R.W., Dworkin, R.H. (2000)Treatment of postherpetic neuralgia: an update. Drugs 59: 5, 1113-1126.

Medinfo. (2003)Shingles. Available at: www.medinfo.co.uk/conditions/shingles.html

Ragozzino, M.W., Melton, L.J., Kurland, L.T. et al. (1982)Population-based study of herpes zoster and its sequelae. Medicine 61: 310-316.

Scott, F. (2000)Shingles: diagnosis and treatment. Nursing Times 96: 50, 36-37.

World Health Organization. (1990)Pain Relief and Palliative Care. Geneva: WHO.

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